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Biomedical subjects

A P Sanders

Publications and source records attributed to A P Sanders.

At least 19 recordsLinked to original sources
PubMed2006

The effects of insole configurations on forefoot plantar pressure and walking convenience in diabetic patients with neuropathic feet.

BACKGROUND: The aim of this study was to evaluate the effects of insole configurations on plantar pressures and on walking convenience in patients with diabetic neuropathy. METHODS: Twelve different insole configurations were constructed for each of 20 patients with diabetic neuropathy. For this, different combinations of a metatarsal dome, varus and valgus wedges and arch supports with different heights were added on a fitted basic insole. Foot orthoses were evaluated while patients walked on a treadmill. Plantar pressure was measured with a Pedar Insole-system. Walking convenience was scored on a 10-point scale. FINDINGS: For the central and medial regions, plantar pressure reductions (up to 36% and 39%, respectively) were found when using a dome, standard and extra supports. The largest reductions were achieved with combination of a dome and extra support. There were no statistically significant pressure reducing effects of the insole configurations in the big toe and lateral regions, except for the effect of the combination extra support/varus wedge (21%), and for a dome (10%), respectively. The basic insole and a standard support received the best ratings for walking convenience and gradually worsened by adding extra support, a varus wedge and a dome. INTERPRETATION: A dome and the supports reduce plantar pressure in the central and medial forefoot. The combination of a dome and extra support seems to be the best choice for the construction of insoles. The results of this study are a step towards developing an evidence-based algorithm for the construction of optimal orthoses in therapeutic shoe design.

Adult↗
PubMed1997

In vivo observations of hydraulic stiffening in the canine femoral head.

The role that intertrabecular contents and their boundary conditions have on the dynamic mechanical response of canine femoral heads was investigated in vivo. Femoral heads from paired intact hind limbs of canine specimens were subjected to a sinusoidal strain excitation at physiologic frequencies, in the cranio-caudal direction. The fluid boundary conditions for the contralateral limbs were changed by predrilling through the lateral femoral cortex and into the femoral neck. The drilling procedure did not invade the head itself. This femoral head fluid boundary alteration reduced the stiffness by 19 percent for testing at 1 Hz. The results of this study demonstrate that fluid stiffening occurs in vivo as previously observed ex vivo.

Animals↗
PubMed1995

Potential for recurrence of hallux valgus after a modified Hohmann osteotomy: a biomechanical analysis.

On the basis of a biomechanical model the present study investigates whether a foot-widening effect, which may result in recurrence of bunions, can be demonstrated in operated patients. Therefore, the medial deviation of the first metatarsal head as a result of flexion forces on the hallux was measured in eight patients with clinical idiopathic hallux valgus, who underwent a modified Hohmann osteotomy, and in eight "normal" persons. We found that (1) before osteotomy, all forefeet broadened while pressing the big toe downward, and (2) after surgery, widening of the forefeet on average had significantly diminished, but still existed, which might explain the development of recurrences. (3) After surgery, the patients showed a slight, but statistically nonsignificant, decrease (from 37 N to 25 N) of the isometrically determined average maximal applicable flexion force. These abnormal hallux loads may cause, or result from, a deviation in gait pattern.

Adult↗
PubMed1991

Stiffening of the femoral head due to inter-trabecular fluid and intraosseous pressure.

The mechanical properties of cancellous bone, as measured from bone plug samples have been widely documented. However, few tests have been attempted to explore the effects the intertrabecular contents may have on the load bearing capabilities. In this study, canine femoral heads were subjected to dynamic compressive strain cycles. The femoral heads were tested intact, as well as with disrupted boundary conditions of the continuous, intraosseous fluid space. A significant reduction in mechanical stiffness was observed when the fluid compartment boundary was disrupted by drilling a hole part way into the femoral neck. A finite element model of a typical femoral head showed that the stiffness change was not due to removal of material from the neck, hydraulic effects notwithstanding. Refilling the hole in the neck with saline solution and sealing the boundary restored the stiffness to the intact baseline level. However, an increase in the fluid pressure did not cause a statistically significant increase in the stiffness of the femoral head.

Animals↗
PubMed1985

Effects of continuous-wave, pulsed, and sinusoidal-amplitude-modulated microwaves on brain energy metabolism.

A comparison of the effects of continuous-wave, sinusoidal-amplitude-modulated, and pulsed square-wave-modulated 591-MHz microwave exposures on brain energy metabolism was made in male Sprague-Dawley rats (175-225 g). Brain NADH fluorescence, adenosine triphosphate (ATP) concentration, and creatine phosphate (CP) concentration were determined as a function of modulation frequency. Brain temperatures of animals were maintained between -0.1 and -0.4 degrees C from the preexposure temperature when subjected to as much as 20 mW/cm2 (average power) CW, pulsed, or sinusoidal-amplitude modulated 591-MHz radiation for 5 min. Sinusoidal-amplitude-modulated exposures at 16-24 Hz showed a trend toward preferential modulation frequency response in inducing an increase in brain NADH fluorescence. The pulse-modulated and sinusoidal-amplitude-modulated (16 Hz) microwaves were not significantly different from CW exposures in inducing increased brain NADH fluorescence and decreased ATP and CP concentrations. When the pulse-modulation frequency was decreased from 500 to 250 pulses per second the average incident power density threshold for inducing an increase in brain NADH fluorescence increased by a factor of 4--ie, from about 0.45 to about 1.85 mW/cm2. Since brain temperature did not increase, the microwave-induced increase in brain NADH and decrease in ATP and CP concentrations was not due to hyperthermia. This suggests a direct interaction mechanism and is consistent with the hypothesis of microwave inhibition of mitochondrial electron transport chain function of ATP production.

Adenosine Triphosphate↗
PubMed1984

The effects of hyperthermia and hyperthermia plus microwaves on rat brain energy metabolism.

The effects of hyperthermia, alone and in conjunction with microwave exposure, on brain energetics were studied in anesthetized male Sprague-Dawley rats. The effect of temperature on adenosine triphosphate concentration [ATP] and creatine phosphate concentration [CP] was determined in the brains of rats that were maintained at 35.6, 37.0, 39.0, and 41.0 degrees C. At 37, 39, and 41 degrees C brain [ATP] and [CP] were down 6.0, 10.8, and 29.2%, and 19.6, 28.7, and 44%, respectively, from the 35.6 degrees C control concentrations. Exposure of the brain to 591-MHz radiation at 13.8 mW/cm2 for 0.5, 1.0, 3.0, and 5.0 min caused further decreases (below those observed for 30 degrees C hyperthermia only) of 16.0, 29.8, 22.5, and 12.3% in brain [ATP], and of 15.6, 25.1, 21.4, and 25.9% in brain [CP] after 0.5, 1.0, 3.0, and 5.0 min, respectively. Recording of brain reduced nicotinamide adenine dinucleotide (NADH) fluorescence before, during, and after microwave exposure showed an increase in NADH fluorescence during microwave exposure that returned to preexposure levels within 1 min postexposure. Continuous recording of brain temperatures during microwave exposures showed that brain temperature varied between -0.1 and +0.05 degrees C. Since the microwave exposures did not induce tissue hyperthermia, it is concluded that direct microwave interaction at the subcellular level is responsible for the observed decrease in [ATP] and [CP].

Adenosine Triphosphate↗
PubMed1984

The differential effects of 200, 591, and 2,450 MHz radiation on rat brain energy metabolism.

Three key compounds in brain energy metabolism have been measured during and after exposure to continuous wave radiofrequency radiation at 200, 591, and 2,450 MHz. Frequency-dependent changes have been found for all three compounds. Changes in NADH fluorescence have been measured on the surface of a surgically uncovered rat brain during exposure. At 200 and 591 MHz, NADH fluorescence increased in a dose-dependent manner between approximately 1 and 10 mW/cm2, then became constant at higher exposures. There was no effect at 2,450 MHz. Levels of ATP and CP were measured in whole brain after exposure. The ATP levels were decreased at 200 and 591 MHz but not at 2,450 MHz. The CP levels decreased only at 591 MHz. The effect of duration of exposure (up to 5 min) was investigated for all compounds at 200 MHz and 2,450 MHz, and exposures to 20 minutes were examined at 591 MHz. Temperature in the rat brain was essentially constant for all exposures. A general mechanism for inhibition of the mitochondrial electron transport chain and the CP-kinase reaction pathway by radiofrequency radiation has been proposed.

Adenosine Triphosphate↗
PubMed1980

Microwave effects on energy metabolism of rat brain.

Rat brain was exposed to 591-MHz, continuous-wave (CW) microwaves at 13.8 or 5.0 mW/cm2 to determine the effect on nicotinamide adenine dinucleotide, reduced (NADH), adenosine triphosphate (ATP) and creatine phosphate (CP) levels. On initiation of the in vivo microwave exposures, fluorimetrically determined NADH rapidly increased to a maximum of 4.0%-12.5% above pre-exposure control levels at one-half minute, than decreased slowly to 2% above control at three minutes, finally increasing slowly to 5% above control level at five minutes. ATP and CP assays were performed on sham- and microwave-exposed brain at each exposure time. At 13.8 mW/cm2, brain CP level was decreased an average of 39.4%, 41.1%, 18.2%, 13.1%, and 36.4% of control at exposure points one-half, one, two three, and five minutes, respectively, and brain ATP concentration was decreased an average of 25.2%, 15.2%, 17.8%, 7.4%, and 11.2% of control at the corresponding exposure periods. ATP and CP levels of rat brain exposed to 591-MHz cw microwaves at 5mW/cm2 for one-half and one minute were decreased significantly below control levels at these exposure times, but were not significantly different from the 13.8 mW/cm2 exposures. For all exposures, rectal temperature remained constant. Heat loss through the skull aperture caused brain temperature to decrease during the five-minute exposures. This decrease was the same in magnitude for experimental and control subjects. Changes in NADH, ATP, and CP levels during microwave exposure cannot be attributed to general tissue hyperthermia. The data support the hypothesis that microwave exposure inhibits mitochondrial electron transport chain function, which results in decreased ATP and CP levels in brain.

Adenosine Triphosphate↗
PubMed1980

A common denominator in the etiology of adult respiratory distress syndrome.

The initiating factor in ARDS is a matter of controversy. Some investigators relate ARDS development to diffuse pulmonary microemboli after stress ranging from sepsis to non-thoracic and thoracic trauma. Others indicate hyperoxic exposure as the causative agent. This investigation looked for a common factor in ischemia and hyperoxic exposure in lung which could cause the genesis of ARDS. Studies of oxidative phosphorylation, succinate dehydrogenase activity and ATP level were performed on ischemic and 100% O2 exposed lung. Results in both showed decreased respiration rate below the basal rate, decreased SDH activity, followed by marked decrease in ATP levels in pulmonary tissue. Decrease in respiration (ATP production) capacity and ATP levels in ischemic lung were such that normal cell functions could not be sustained if returned to normal circulation. Hyperbaric O2 therapy would subsequently decrease energy metabolism in regions of normal circulation and in previously ischemic regions.

Adenosine Triphosphate↗